Toymaker Television

Daily content for the geek and DIYer

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Context is everything

Just as a follow-up to this article, I haven’t been through the ENTIRE process, but have certainly been witness to what it all involves.  Essentially after writing a paper, you send it off to a journal, who then chooses 3-4 reviewers from your field to review your paper.  They rip it to shreds, find what data still needs to be done, and then come back with their red pen telling you what’s what.  That’s called a peer-review.  And you either rebutt or you add on to your research to answer their questions.

The reason peer-review is important is because while YOU may be convinced about the results and what the results mean, your job as a scientist is to demonstrate proof to others who are equally qualified to analyze your data.  The peer reviewer is meant to make your data become above-reproach.

So it was interesting when I read this comment, in response to the article I’ve been reading through:

This team expressed quite a few concerns about the article, many of them which I have not vetted, but is worth considering because it largely considers the study negligent and over-exaggerating of its results.  It’s all because of context.  I’d advise you take some time to read through the answer, it’s pretty interesting and informative.

This also touches on why I think it’s interesting that this particular study, performed at a rather prestigious center, would send this sort of article to PLOS One as opposed to a more well known journal.  Because if indeed this data is sound and if the technique is sound, then it has fairly significant findings that a journal would be happy to pick up.  

The following is the peer review “About Us” for PLOS ONE: “Often a journal’s decision not to publish a paper reflects an editor’s opinion about what is likely to have substantial impact in a given field. These subjective judgments can delay the publication of work that later proves to be of major significance. PLOS ONE will rigorously peer-review your submissions and publish all papers that are judged to be technically sound. Judgments about the importance of any particular paper are then made after publication by the readership, who are the most qualified to determine what is of interest to them.”

I don’t know what kind of peer review this went through, but from the one review done by the commenter, it seems not enough.


Filed under the flip side tymkrs peer review plos one ritalin dopaminergic neuron dopaminergic system chronic ritalin

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Ritalin and Dopaminergic System Part 6

Following article courtesy of @lmcomie:

Sadasivan, S., Pond, B.B., Pani, A.K., Qu, C., Jiao, Y., & Smeyne R.J. (2012) Methylphenidate Exposure Induces Dopamine Neuron Loss and Activation of Microglia in the Basal Ganglia of Mice. PLOSONE, 7(3).

Last post about this article!  I finally found some time to go through the materials and methods.  So St. Jude Children’s Research Hospital was where this research was done.  The mice were 3 weeks old and maintained on a 12h light/dark cycle (this is normal).  Starting when they were 28 days (this is about young adulthood/just off weaning), they were given injectsion of saline, 1mg/kg or 10mg/kg Ritalin at 5pm - 1 hour before their active nocturnal phase at 6pm.

Doses were chosen sbased on previous studies in rodents suggesting that Ritalin doses of < 5mg/kg mirror those that are used in clinical practice, as opposed to recreational and narcoleptic use = dose of 10mg/kg.

Ritalin injections were given 5 days a week and at the end of the 12 weeks, the animals were allowed a washout period of a week.

After the week of washout, the mice were anesthetized and euthanized.  The method they describe is fairly common for brain analysis.  And then the brain was sliced to 10um thick for analysis.  I can’t tell if they had to count neurons by eye or not, but they mentioned using a “optical fractionator method” - it may be some sort of estimating tool developed with a specific microscope in mind.

For MPTP treatment, the final concentration was 5mg/ml and each animal was given 4 injections of 20 mg/kg MPTP - one every 2 hours for 8 hours.  All mice then stayed around for a week after the injections, before euthanization.

The rest of the article describes the methods they used for measuring mRNA and expression signals - unfortunately not my forte - but still a well documented method in many different studies.

I think one thing to note is that the n levels (number of subjects) that they tested throughout these experiments is relatively low compared to how many mice are usually put through an experiment.  The n numbers are anywhere from 3 to 8.  This is not very high.  IE. They’re using the results from 3 mice to come to this conclusion.  The research would have been much stronger had there been at least 10 mice per category.  The logistics, however, would have been difficult.  (Why? Cuz mice don’t like injections anymore than humans do)


Filed under tymkrs ritalin dopaminergic neuron methylphenidate chronic ritalin parkinsons methods

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Ritalin and Dopaminergic System Part 5

Ritalin and Dopaminergic System Part 5

Following article courtesy of @lmcomie:

Sadasivan, S., Pond, B.B., Pani, A.K., Qu, C., Jiao, Y., & Smeyne R.J. (2012) Methylphenidate Exposure Induces Dopamine Neuron Loss and Activation of Microglia in the Basal Ganglia of Mice. PLOSONE, 7(3).

The discussion section is like the summary section with a “why did we get the results we got” added in.  So if a lot of this looks familiar, it’s probably because it is!

Alright, so they do a study looking at the effects of an ADHD and Narcolepsy dose of Ritalin.  They found that giving both doses chronically makes dopaminergic neurons in the substantia nigra, a location in the brain involved in reward, addiction, and Parkinson’s, more susceptible to further stress.  And it does it by increasing the number of inflammatory factors that are activated/created and decreasing the factors that are usually responsible for creating new neurons, more dopamine, etc.

Specifically, they used a 3 month Ritalin schedule that spans the developmental period in mice and corresponds to the pre-adolescent through young adult period in humans, during which Ritalin’s usually used.

Usually Ritalin works by increasing the amount of dopamine and norepinephrine in the brain by blocking the proteins that take back dopamine and norepi once they’ve finished their actions.  In the study, they saw that there was a significant increase in dopamine levels at the ADHD dose, one that was not seen at the narcolepsy dose.  Other small doses that have been studied have also seen this increase in dopamine levels.  

The lack of change in dopamine at the higher level may be because of chronic dosing of the drug, or maybe some sort of compensatory change in the production of dopamine due to there being fewer neurons.  So they measured the ratio of dopamine to dopaminergic neurons.  Interestingly, when examined as a ratio, both the 1 and 10mg/kg doses showed a significant increase in the dopamine:neuron ratios - 150% in 1mg/kg and a 132% increase in 10mg/kg Ritalin.  This suggests that both doses increase dopamine levels, not just that of 1 mg/kg.

Of course, increased extracellular dopamine may be a problem.  Oxidation of dopamine can produce a whole bunch of superoxides and in turn radicals.  Neurotoxins abound!  And as mentioned before, they hypothesized that chronic Ritalin would cause the neurons to be more sensitive to a later stress.  So they gave MPTP, an agent that is known to induce oxidative stress (one that normally does not induce any stress on the particular strain of mouse they had).  They found that chronic exposure to both doses increased the sensitivity of the neurons to oxidative stress - based on the fact that both doses lost neurons when given Ritalin and MPTP as compared to saline.

They also found that there was a significant increase in Ritalin-induced microglia - so they think that perhaps, an increase in radical formation from increased dopamine levels + a neuroinflammatory response (increase in microglia) increases the sensitivity of the dopamine neurons to a later oxidative challenge.

They wanted to see if there were any specific explanations for why the neurons were more sensitive to oxidative stress after having been given Ritalin.  Through genetic analysis, they saw that there were a number of genes that changed their level of expression after both 1 and 10mg/kg doses.  These were mostly related to inflammation and cell damage and repair pathways.  They found a decrease in expression of genes involved in dopamine synthesis and handling - again after both doses of Ritalin.

They found that short term exposure to higher doses of Ritalin increased the expression of inflammatory genes in the striatum.  Surprisingly they did not find an increase in inflammatory gene expression after chronic administration of Ritalin, though there was still an increase in activated microglia.  This suggests that sometime during the course of the chronic Ritalin, there may be some sort of repression of inflammatory gene expression.

Unknown if the gene repression after chronic treatment with Ritalin is permanent or if it can be later re-induced.  If this is the case, then the activated microglia may potentially play a modulatory role in inducing oxidative stress.  Or perhaps the microglia that are activated are not able to return to their pre-inflamed state.

So all together, this study suggests that chronic Ritalin in mice results in a reduced expression of neurotrophic factors (creation/healing), increased inflammation, and a loss of dopamine neurons.

Tomorrow, the methods! (Arguably one of the most important sections)


Filed under tymkrs dopaminergic neurons ritalin chronic ritalin neuroinflammation methylphenidate mrna expression neurotrophins dopamine

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Ritalin and Dopaminergic System Part 4

Following article courtesy of @lmcomie:

Sadasivan, S., Pond, B.B., Pani, A.K., Qu, C., Jiao, Y., & Smeyne R.J. (2012) Methylphenidate Exposure Induces Dopamine Neuron Loss and Activation of Microglia in the Basal Ganglia of Mice. PLOSONE, 7(3).

The wording keeps getting more and more jargony! Please be sure to check out parts 1, 2, and 3

Alterations in Gene Expression following Acute and Chronic MPH Exposure in SN:

They wanted to see whether there were any changes to gene expression and see what the genes were for.  They found that expression of 115 genes had changed between saline and the 1mg/kg Ritalin dose and expression of 54 genes had changed between saline and the 10mg/kg Ritalin dose.  Of these genes, 23 were expressing differently between the lower and higher Ritalin dose.

Since the larger changes in neuronal number and microglia (cells involved in fixing the brain after traumatic brain injury) occurred with the higher dose, they wanted to look at the gene expression in mice with only this dose.  They looked at specific genes associated with basal ganglia toxicity (note: the basal ganglia consists of structures involved in control of voluntary motor movements, procedural learning, routine behaviors or “habits”, eye movements, cognition and emotion) including:

  • brain derived neurotropic factor (bdnf): support survival of neurons and growth of new ones
  • glial derived neurotopic factor (gdnf): promotes survival and differentiation of dopaminergic neurons
  • tyrosine hydroyxlase (th): creates precursors of dopamine (L-DOPA specifically)
  • dopamine transporter DAT1 (slc6a3): recycles dopamine
  • vesicular monoamine transporter VMAT2 (slc18a2): membrane protein that transports neuropeptides like dopamine

They found significant decreases in mRNA expression in gdnf, th, slc6a3, and slc18a2 after both acute and chronic administration of 10 mg/kg Ritalin while bdnf was only reduced after chronic 10 mg/kg Ritalin. 

  • Note - mRNA turns into proteins.  It’s like a template that proteins get copied off of.  If there’s less mRNA, there’re fewer proteins that it’s making.

Again, I think it would have been much more interesting had they also included the 1mg/kg dose and those results, even if they were no different than the saline mice.

Evidence for inflammation associated with acute doses of MPH:

They also wanted to see if since there was an increase in activated microglia following the higher dose of Ritalin, they wanted to see whether inflammatory genes had changed expression as well.  Specifically:

  • il-6: signaling protein that is usually activated in burn/tissue damage traumas
  • tnf-alpha: regulates immune cells by inducing fever or even cell death
  • cox-2: causes fevers in response to immune system attack
  • il1b: involved in cell proliferation, cell differentiation and cell death

They found that there were significant increases in mRNA expression of tnf-alpha and il-6 in those given a single dose of 10mg/kg MPH as compared to saline-injected mice.

And these were the results!  Tomorrow we’ll start on the discussion section - which is usually where the researchers talk about why they think they saw what they saw.



Filed under dopaminergic system tymkrs dopamine research chronic ritalin ritalin methylphenidate inflammation gene expression ritalin in mice adhd narcolepsy

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Ritalin and Dopaminergic System Part 3

Still reading through the following article courtesy of @lmcomie:

Sadasivan, S., Pond, B.B., Pani, A.K., Qu, C., Jiao, Y., & Smeyne R.J. (2012) Methylphenidate Exposure Induces Dopamine Neuron Loss and Activation of Microglia in the Basal Ganglia of Mice. PLOSONE, 7(3).

There are more results! Chronic MPH exposure sensitizes the SNpc to MPTP effects:

So since the higher dose of Ritalin (given over 90 days) lowered the dopaminergic neuron number in the substantia nigra, they wanted to see whether it also increased the sensitivity of the neurons to a parkinsonian agent MPTP.  That is, would giving MPTP after Ritalin cause the brain to be more likely to be in a state of stress and would there be additional dopaminergic neuronal death.

  • Reminders: Substantia nigra is a region of the brain involved in reward, addiction, and decreased neuron levels in this area lead to Parkinson’s.
  • MPTP is a neurotoxin precursor to MPP+, which causes permanent symptoms of Parkinson’s disease by destroying dopaminergic neurons in the substantia nigra.

It’s interesting to note that normally these type of mice are not affected by MPTP and do not lose any neurons as a result of receiving this agent.  SO, whichever ones ARE lost, are because of the presence of Ritalin.

So what they found was that giving 1mg/kg or 10mg/kg of Ritalin DID make the neurons more sensitive to MPTP.  That is, where previously they would not have been damaged, they were now.  And MPTP was able to induce a 20% increase in cell death in mice that had RItalin.

They also looked to see how the microglia (cells involved in cleaning/fixing up after a brain injury) reacted to Ritalin and MPTP.  Since only an increase in activated microglia was seen in mice with the higher dose, they only gave this group MPTP (I think they should have given it with the 1mg/kg group as well).  And found that those given 10mg/kg Ritalin + MPTP showed a decrease in the number of resting microglia and a rise in the number of activated microglia.

Note that the increase in dopaminergic neuron loss was not large enough to result in the onset of parkinsonism, but certainly is a factor that should be considered in neurodegenerative disorders that involved the dopaminergic system.


Filed under tymkrs dopaminergic system dopamine neurons mptp mph ritalin chronic ritalin neuroscience

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Ritalin + Dopaminergic System Part 2

I’m currently reading through the following article courtesy of @lmcomie:

Sadasivan, S., Pond, B.B., Pani, A.K., Qu, C., Jiao, Y., & Smeyne R.J. (2012) Methylphenidate Exposure Induces Dopamine Neuron Loss and Activation of Microglia in the Basal Ganglia of Mice. PLOSONE, 7(3).

We just went through the introduction yesterday, and now for results! (Usually methods comes next, but the authors chose to go results first).

Chronic MPH administration affects SNpc DA neuron number:

So we finally hear what they found out.  They looked at the substantia nigra pars compacta, a region of the brain that has been associated with reward, addiction, and degeneration of which is linked to Parkinson’s Disease.  They looked to see what would happen in this region of the brain with chronic exposure (90 days) to saline vs 1mg/kg (ADHD dosage) vs 10 mg/kg (narcolepsy/recreational dosage) - specifically the number of dopaminergic neurons.

They found that for the mice treated with 1mg/kg there was not any difference from the saline (control group) but that in those treated with 10mg/kg for the 90 days had a 20% reduction of dopaminergic neurons in the substantia nigra.  And that it was the neurons towards the back of the substantia nigra that was affected more than those in the front.  The significance of that is (as far as I can tell from a cursory search), still being studied.


The red arrows highlight dopamine neuronal counts for mice with just saline, 1mg/kg, and 10mg/kg Ritalin.  The second graph shows the distance from front to back of the substantia nigra and how many neurons were found in those different sections.

Chronic MPH exposure results in microglia activation in the SNpc:

So as we’ve mentioned a couple of times while reading this study, excess dopamine causes the brain to be in an inflamed and stressed out state.  The scientists wanted to see if chronic Ritalin could induce a reaction similar to that of excess dopamine by measuring the number of resting and active microglia.  

  • Remember that excess dopamine causes release of signaling pepties (cytokines/chemokines) that cause microgliosis (scar formation, new neuron formation, but also production of toxic factors.

What they found was that giving the 1mg/kg (ADHD dose) Ritalin didn’t change any microglia numbers.  And while giving 10mg/kg (narcolepsy dose) Ritalin did not change the number of resting microglia, it did cause a significant increase of activated microglia.  This suggests that there was some form of stress/inflammation occurring, otherwise those microglia would not have activated.


The red arrows point to saline vs 1mg/kg vs 10mg/kg Ritalin.  On the left graph are the resting microglia and the right graph are the activated microglia.  No difference in resting, but statistically significant difference with the 10mg/kg dose of Ritalin.

Dopamine and dopamine turnover affected following chronic MPH dosing:

Then they wanted to see if chronic administration of Ritalin resulted in changes in total striatal dopamine levels or dopamine turnover.

  • Note: The striatum feeds the basal ganglia, all of the parts of the brain that are responsible for control of voluntary motor movements, procedural learning, routine behaviors, eye movements, cognition, and emotion
  • Note: Classically, dopamine turnover is defined as the ratio between dopamine metabolites and dopamine itself.  I think of it as dopamine’s lego-building blocks as opposed to the dopamine itself.  From a quick glance around other articles, an increase in dopamine turnover has been hypothesized to occur early in Parkinson’s disease (PD) as a compensatory mechanism for dopaminergic neuronal loss.  So not a great thing to have, but maybe one of the first lines of defense.  Get rid of the excess dopamine by changing it to its metabolites, save the neuron!

They found that long-term 1mg/kg increased total striatal dopamine compared to saline but that long-term 10mg/kg did not.  And there was a significant increase in major dopamine metabolite named DOPAC at both Ritalin doses.  Luckily (or maybe not) only the 10mg/kg MPH dose saw an increase in dopamine turnover.  So 1mg/kg did not seem to be enough to trigger the dopamine becoming all of its metabolites although there was an increase in DOPAC. (See note after graph)


In looking at the graphs, we can see % dopamine did increase in the 1mg/kg dose but not the 10mg/kg dose.  And that in both 1mg/kg and 10mg/kg doses, there’s an increase in DOPAC.  But it seems that the scientists may have misread graph C because according to this graph, it seems that both 1mg/kg and 10mg/kg MPH have significantly increased turnover as compared to Saline.

I may have to write them asking them! More tomorrow!  (Also this is why it’s important to read the graphs, and not just what is written about them!)


Filed under substantia nigra tymkrs chronic ritalin mph dopaminergic neuron caudal mph exposure microglia activated microglia resting microglia DOPAC dopamine metabolite dopamine turnover neuroscience neuropharmacology

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Ritalin + Dopaminergic System Part 1

Local buddy (though not for long) @lmcomie linked to an interesting article yesterday regarding Ritalin exposure and its effects on the basal ganglial system in mouse models.  So I thought I’d break down the article, and see what all it was saying, but maybe from a more reader-friendly perspective. Here’s the citation and location of the article:

Sadasivan, S., Pond, B.B., Pani, A.K., Qu, C., Jiao, Y., & Smeyne R.J. (2012) Methylphenidate Exposure Induces Dopamine Neuron Loss and Activation of Microglia in the Basal Ganglia of Mice. PLOSONE, 7(3). 


Ritalin has been prescribed for the management of ADHD and narcolepsy.  It’s been shown to be addictive and an increasing number of adults/college students are using it for “cognitive enhancement”.  A number of students feel Ritalin helps them “super-concentrate” so they are using it without regards for why it was brought on the market in the first place.

Previous studies have shown that in both ADHD and non-ADHD populations, Ritalin has been shown to increase scores on tests as well as increase working memory, and people have asked for it to become an over-the-counter drug.  But few studies have been published demonstrating the long-term consequences of using Ritalin.

Ritalin is a stimulant that blocks the dopamine transporter and norepinephrine transporter - much like cocaine.  

  • Note: Transporters are involved in the recycling of signaling neuropeptides.  So when your body signals that dopamine needs to be released, the neurons release them into the gap between neurons known as the synapse.  When they’re done sending the message to the next neuron, transporters vacuum the dopamine back up (or any other neuropeptide), and save them for another day.  So by blocking the dopamine and norepi transporters, you end up with dopamine and norepi staying longer in those synapses, and therefore they act longer on the recipient neurons.

So Ritalin usage leads to an increase in dopamine levels but, be warned, excess levels of dopamine are toxic as it produces superoxide, hydrogen peroxide, and dopamine quinone.  

  • Those are some of the same items that your white blood cells use to kill invading microorganisms.  Great when they’re being controlled by your white blood cells, toxic otherwise.  

Free ranging dopamine has also been shown to cause inflammation to occur in the brain which is shown by an increase in cytokines and chemokines - cell signaling proteins that say “Hey! Brain inflammation going on, take care of it!”  

Microgliosis is one of the processes induced by the increase in these signaling proteins and usually occurs when a person has a brain injury.  It involves microglial cells coming to the site of the injury, getting rid of any germs, getting rid of any dead/damaged neurons, and encourage growth of new neurons.  But, overactivation of the microglial cells leads to production of a number of toxic substances as well as inflammatory factors.

So, this study looks at whether long-term Ritalin usage in mice at 2 doses induces changes in the basal ganglia.  Per wiki, the basal ganglia consists of regions involved in control of voluntary motor movements, procedural learning, routine behaviors, eye movements, cognition, and emotion.  Interesting to note is that the dosages used in the mice - 1mg/kg and 10mg/kg - reflect the prescribed dosages that humans would receive for ADHD and recreational use/narcolepsy (respectively).

  • That is, 1mg/kg = ADHD and 10mg/kg = Narcoplepsy/Recreational 

They looked to see if short term or long term Ritalin changed dopamine neuron numbers and dopamine levels in the substantia nigra portion of the brain.  And since excessive dopamine has been shown to induce inflammation (as mentioned above), they looked to see if after Ritalin, neurons would be more sensitive to a drug MPTP that has been shown to cause neuron damage.

  • Note: substantia nigra is a portion of the brain that plays a role in reward, addiction, and movement.  Loss of dopaminergic neurons in this area leads to Parkinson’s Disease.

Results tomorrow!


Filed under tymkrs substantia nigra dopamine dopaminergic system ritalin methylphenidate chronic ritalin transporters neuropeptides neuroscience

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RoadTrip Day 13: Miles and Miles and Miles…

So the trip home is like….18-20 hours. This means there are a few options, either we split the driving half-half, or we go hardcore today and easy tomorrow. DELAYED GRATIFICATION!

So we did the latter. I’m currently in the Best Western in Topeka and we drove 13 hours. 7:30 - 9:00 essentially. According to the map, with all of our breaks, we only actually covered 11 hours worth. BAH!

It looks like tomorrow, we have anywhere from 7-8 hours worth of driving *falls over*


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RoadTrip Day 12: More ABQ!

Today was fun :) We woke up in Albuquerque after a night of burgers at The Cube, and Whisker and I played around with music, him on his acoustic, and me on Kumi’s new mandolin - a very fun instrument. We ended up with an instrumental track we’ll be including in our album so yay!

Bugged Kumi to go to sushi which we devoured. Really quite good sushi in ABQ, even with green chile on it. We then went to get some green chiles and bought a 1/4 of a bushel for like…8 bucks. It was amazing. And there are a crapton lol. They offered to roast it, but I kinda want to do it for posterity’s sake.

Let’s see….then we went back, recorded the track we had been playing around on, and when that was done, totally made Kumi watch Escanaba in da Moonlight. Truly one of the strangest movies I know, yet strangely educational about the Michigander.

We then went to eat some tasty foods at El Patron, and I had the Baja Fish Tacos which were super tasty, yay for chipotle aioli sauce! Whisker got the blue corn enchiladas with green chiles - spicyyy…We also met Kumi’s sister which was awesome :D.

Once getting back, I totally went fishing Wii style with Kumi. Whisker read a book, and eventually fell asleep to the sounds of the ocean. Meanwhile, I’m busy reeling in 4 foot fish *rah rah rah* :) I love fishing, especially fishing in games lol.

Sadly tomorrow we have to leave, so. :(


Filed under roadtrip tymkrs

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RoadTrip Day 11: 59 in a 55…punks.

So, this morning we got up super early, sadly left John’s wonderful paradise, and made our way out onto 60E. I think 60 E is a more beautiful unveiling of the landscape than 60W, so I definitely took advantage of the views. But on our way through the little towns, and back into the middle of nowhere, I passed a cop car going, apparently, 59 in a 55, or so he says as his lights flash in my rear view mirror.

This is literally the middle of nowhere, and I was the only car around for hours. So he tells me why he’s stopped me. And I’m sure he’s surprised because as he sticks his head into the car, we’re playing big band swing music via CD.

"What can I do for you officer?"
“You were going 59 in a 55”
*shock* “I was?!” (actually I didn’t have a clue it was a 55 zone, I was pretty sure it was a 65 zone)
“I’ll write you up a warning this time, just slow it down.”
“Yes sir…”
“Can I get your license and registration?”
“Sure” *pulls out all that stuff*
“Can you step out of the car while I process this?”
“Uh sure…” (why do they have you step out of the car?) So I get out and stand by him watching him write this damn warning down.
“So where’re you headed?”
“Albuquerque, NM”
“Oh wow, that’s far! What’re you doing there?”
“We’re on a roadtrip from Minnesota” *listed out the different places we had been*
“So what’re you doing on a roadtrip?”
“Ah okay, and what do you do?” (I’m thinking he’s asking too many questions but whatever)
“I’m a nurse.” (Yeah jackass, you pulled over a nurse)
“Oh cool.” (Yeah jackass, you still pulled over a nurse)
“And who else is in the vehicle?”
“My boyfriend and a friend.” (does it matter?)
“Oh okay, and what does your friend do?”
“She refurbishes computers. She essentially works at a nonprofit that helps disabled individuals with becoming more independent.” (Totally true, and you jackass, you stopped a car that had good citizens in it)
“Oh neat.” He totally gets quieter at this point cuz you know, there’re other nefarious folks on the road to pick on!
“So this is a vacation huh?”
“Yep, first one in a while” (I had to ham this one up since we had one in May, didn’t want him thinking better of himself)
“And I’ve never even been pulled over in my entire life before!”
“No? Never?”
“Nope, never. Feel free to you know, skip the Minnesota plates!”
“Well I gotta pull someone over. And at least it’s just a warning and not in Phoenix, cuz it’s hot there!” (What is this, a silver lining in the pull-over cloud?)
He starts squinting and furrowing his brow at the license plate.
“Is this your car?”
“Yeah, it’s a leased car, I just got it a month or so ago.”
“Oh, and are these plates your’s?” (I’m pretty sure he was contemplating they were stolen)
“Yes….I just got those a couple of weeks ago.”
“Oh. Are they plates from the last owner of the vehicle?”
“Nope, they’re my plates for this car. I just got them from the dealership.”
“So you got a new car for the roadtrip?”
“No…I got a new car cuz it was time to switch out my lease.”
“Oh. Oh there it goes.”
“Sorry, the information from Minnesota comes up differently.”
“No problem” (jackass!)
“Alright, here you go, here’s your registration and license.”
“Have a good day”
“Thanks, you too.”


We end up at VLA where there is a serious grasshopper problem. Like…MILLIONS of the creatures. We’ll show you guys footage, it’s a little scary. But do you think the gift shop was open? NOPE! Closed till Thursday for inventory! wtf. I’m pretty sure I heard voices there so I knocked. They hushed up. Double punks!


Filed under roadtrip tymkrs